The rapid scientific interest in gut microbiota (GM) has coincided with a global increase in the prevalence of infectious and non-infectivous liver diseases. GM, which is also called “the new virtual metabolic organ”, makes axis with a number of extraintestinal organs, such as kidneys, brain, cardiovascular, and the bone system. The gut-liver axis has attracted greater attention in recent years. GM communication is bi-directional and involves endocrine and immunological mechanisms. In this way, gut-dysbiosis and composition of “ancient” microbiota could be linked to pathogenesis of numerous chronic liver diseases such as chronic hepatitis B (CHB), chronic hepatitis C (CHC), alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), development of liver cirrhosis, and hepatocellular carcinoma (HCC). In this paper, we discuss the current evidence supporting a GM role in the management of different chronic liver diseases and potential new therapeutic GM targets, like fecal transplantation, antibiotics, probiotics, prebiotics, and symbiotics. We conclude that population-level shifts in GM could play a regulatory role in the gut-liver axis and, consequently, etiopathogenesis of chronic liver diseases. This could have a positive impact on future therapeutic strategies.

Hospital-acquired infections (HAIs) are a global public health concern. As the COVID-19 pandemic continues, its contribution to mortality and antimicrobial resistance (AMR) grows, particularly in intensive care units (ICUs). A two-year retrospective study from April 2019–April 2021 was conducted in an adult ICU at the Hospital for Infectious and Tropical Diseases, Belgrade, Serbia to assess causative agents of HAIs and AMR rates, with the COVID-19 pandemic ensuing halfway through the study. Resistance rates >80% were observed for the majority of tested antimicrobials. In COVID-19 patients, Acinetobacter spp. was the dominant cause of HAIs and more frequently isolated than in non-COVID-19 patients. (67 vs. 18, p = 0.001). Also, resistance was higher for imipenem (56.8% vs. 24.5%, p < 0.001), meropenem (61.1% vs. 24.3%, p < 0.001) and ciprofloxacin (59.5% vs. 36.9%, p = 0.04). AMR rates were aggregated with findings from our previous study to identify resistance trends and establish empiric treatment recommendations. The increased presence of Acinetobacter spp. and a positive trend in Klebsiella spp. resistance to fluoroquinolones (R² = 0.980, p = 0.01) and carbapenems (R² = 0.963, p = 0.02) could have contributed to alarming resistance rates across bloodstream infections (BSIs), pneumonia (PN), and urinary tract infections (UTIs). Exceptions were vancomycin (16.0%) and linezolid (2.6%) in BSIs; tigecycline (14.3%) and colistin (0%) in PNs; and colistin (12.0%) and linezolid (0%) in UTIs. COVID-19 has changed the landscape of HAIs in our ICUs. Approval of new drugs and rigorous surveillance is urgently needed.

Chronic pulmonary aspergillosis (CPA) is a chronic progressive lung disease associated with a poor prognosis and a 5-year mortality rate of approximately 40–50%. The disease is characterized by slowly progressive destruction of the lung parenchyma, in the form of multiple cavities, nodules, infiltrates or fibrosis. CPA can be challenging to diagnose due to its non-specific symptoms and similarities with other respiratory conditions combined with the poor awareness of the medical community about the disease. This can result in delayed treatment even for years and worsening of the patient’s condition. Serological tests certainly play a significant role in diagnosing CPA but cannot be interpreted without radiological confirmation of CPA. Although many data are published on this hot topic, there is yet no single definitive test for diagnosing CPA, and a multidisciplinary approach which involves a combination of clinical picture, radiological findings, microbiological results and exclusion of other mimicking diseases, is essential for the accurate diagnosis of CPA.

Considering the relevance of the research of pathogenesis of different liver diseases, we investigated the possible activity of the IL-23/IL-17 axis on the immunohepatotoxicity of two etiologically different chronic liver diseases. A total of 36 chronic hepatitis C (CHC) patients, 16 with (CHC-SF) and 20 without significant fibrosis (CHC-NSF), 19 patients with non-alcoholic steatohepatitis (NASH), and 20 healthy controls (CG) were recruited. Anthropometric, biochemical, and immunological cytokines (IL-6, IL-10, IL-17 and IL-23) tests were performed in accordance with standard procedure. Our analysis revealed that a higher concentration of plasma IL-23 was associated with NASH (p = 0.005), and a higher concentration of plasma IL-17A but a lower concentration of plasma IL-10 was associated with CHC in comparison with CG. A lower concentration of plasma IL-10 was specific for CHC-NSF, while a higher concentration of plasma IL-17A was specific for CHC-SF in comparison with CG. CHC-NSF and CHC-SF groups were distinguished from NASH according to a lower concentration of plasma IL-17A. Liver tissue levels of IL-17A and IL-23 in CHC-NSF were significantly lower in comparison with NASH, regardless of the same stage of the liver fibrosis, whereas only IL-17A tissue levels showed a difference between the CHC-NSF and CHC-SF groups, namely, a lower concentration in CHC-NSF in comparison with CHC-SF. In CHC-SF and NASH liver tissue, IL17-A and IL-23 were significantly higher in comparison with plasma. Diagnostic accuracy analysis showed significance only in the concentration of plasma cytokines. Plasma IL-6, IL-17A and IL-23 could be possible markers that could differentiate CHC patients from controls. Plasma IL-23 could be considered a possible biomarker of CHC-NSF patients in comparison with controls, while plasma IL-6 and IL-17-A could be biomarkers of CHC-SF patients in comparison with controls. The most sophisticated difference was between the CHC-SF and CHC-NSF groups in the plasma levels of IL-10, which could make this cytokine a useful biomarker of liver fibrosis.

In late December 2019, in the city of Wuhan, in China, the appearance of unknown viral pneumonia was recorded in a large number of patients. The cause of this infection was soon discovered - a new coronavirus, called SARS-CoV-2, due to its genetic similarity to the virus that causes severe acute respiratory syndrome (SARS-CoV). The infection then spread rapidly to other continents, and the pandemic is still ongoing. The clinical presentation varies from the asymptomatic form to symptoms of upper respiratory tract infection, and finally to pneumonia and acute respiratory distress syndrome (ARDS). The elderly, immunocompromised patients, and patients suffering from chronic, internal medicine diseases are at risk of the severe form of the COVID-19 disease. The virus enters cells via angiotensin converting enzyme 2 (ACE2) receptors, which are present in practically all tissues in the body. In addition to interstitial pneumonia, pathological changes are also found in other organ systems. The first case in Serbia was recorded on March 6, 2020. A large number of patients required the engagement of health workers of all profiles as well as the introduction of a large number of health institutions into the COVID system. The emergence of a new virus necessitated a new antiviral drug. Based on previous experience with the SARS-CoV virus, previously known antiviral drugs have been used, with varying degrees of success. The therapy changed in accordance with new knowledge, and since the beginning of the epidemic in Serbia, the National Protocol of the Republic of Serbia for the Treatment of the COVID-19 Infection has been established, which has kept apace with the recommendations of the world's leading institutions. The most significant event during the pandemic was the development of the vaccine against COVID-19, with vaccination in Serbia beginning in December 2020. How quickly the epidemic will end depends directly on the speed and efficiency of vaccination, along with other epidemiological measures.

Considering the relevance of the pathogenesis research of different liver diseases, in our study we investigated the possible activity of IL-23/IL-17 axis on the im-munohepatotoxicity of two etiologically different CLD. A total of patients with CHC infection, 19 with NASH and 20 healthy controls (CG) were recruited. After histological verification from liver tissue obtain by liver biopsy, patients with CHC were divided into two groups: CHC-NSF (F0/F1/F2)-non-significant fibrosis, 20 patients, and CHC-SF (F3/F4)-significant fibrosis/cirrhosis, 16 patients. All anthropometric, biochemical, immunological cytokines (IL-6, IL-10, IL-17 and IL-23) tests were performed accordance to standard procedure. The plasma levels of IL-6, Il-17A and IL-23 were significantly higher in CHC-SF and NASH in compared with CG. Also, plasma levels of IL-23/IL-17A were significantly higher in NASH in compared to CHC-SF. In CHC-SF we had significantly lowest IL-10 level in compared with all three groups. Liver tissue levels of IL-17A and IL-23 in CHC-NSF were significantly lower in compared with NASH. IN CHC-SF and NASH, IL17-A and IL-23 in liver tissue were significantly higher in compare to plasma levels. In conclusan, proinflammatory response of IL-23/17A axis is dominant in plasma and liver tissue in CHC with higher levels of liver fibrosis and in NASH patients.